POCUS And Its Utility in the Rapid Diagnosis of Acute Cholecystitis

CASE

A 48-year-old female with a past medical history of hypertension and hyperlipidemia and no past surgical history presented to the ED with constant, sharp, and burning epigastric pain. The pain started two weeks ago and was initially intermittent, centered in the epigastric region. Over the past day or so, the pain worsened and began traveling to the right side of her chest and around to the back. The pain was daily, usually after meals, and made worse by fatty foods. The patient felt slightly better after taking antacids. She reported the pain was 8/10 at worst, typically lasting several hours at this intensity, and receded to 3/10 at its best. She had some nausea but no vomiting. She denied changes in stool consistency/frequency or dark or bloody stools. She denied chest pain, sweating, or palpitations. She reported a subjective fever last night and into this morning, but no chills or change in weight. She had been compliant with her home medications.

On physical exam, vital signs were T:99.8F, systolic blood pressure of 130, HR in the 90s, respiratory rate of 16, and SpO2 of 97% on RA. She appeared uncomfortable but was able to participate in the interview and examination. She had no chest wall tenderness. Lungs were clear. Heart was regular rate and rhythm with no murmurs, rubs or gallops. Bowel sounds were present in four quadrants. She had a soft, nondistended abdomen with tenderness to palpation of the epigastric area and just right of the epigastric region with guarding but no rebound. No obvious hepatosplenomegaly. There were no findings on skin exam. 

Her EKG showed a normal sinus rhythm. CBC revealed mild leukocytosis to 13 with small left shift. Normal lipase. Slightly elevated ALT/AST (80/50), and normal bilirubin and alkaline phosphatase. Troponin <0.04. U/A normal. 

The etiology of her abdominal pain was thought to involve the hepatobiliary system, thus point of care ultrasound was performed in the emergency department. The findings are below:


Multiple stones with shadowing identified in the gall bladder with increased wall thickness and trace surrounding pericholecystic fluid. Positive sonographic Murphy’s sign.  


DIAGNOSIS

Acute Cholecystitis 

DISCUSSION

What is acute cholecystitis?

Acute cholecystitis most often results from a gall stone becoming lodged in the cystic duct, causing the inability of the gall bladder to empty bile into the common bile duct. The attempted constriction against a gall stone causes trauma to the gall bladder wall. It is thought that the interaction of the gall bladder mucosa and the bile itself leads to the creation of a chemical, called lysolecithin. Lysolecithin acts as an irritant to the gall bladder, leading to further inflammation.[1]

It is important to include in the differential for acute cholecystitis other pathologies that can cause pain in the right upper quadrant. Chief among the other possible hepatobiliary causes is ascending cholangitis, a life-threatening condition, which results from stasis and infection of the biliary tract. This can be caused by a gall stone blocking the common bile duct (choledocholithiasis), a bile duct stricture, malignancy, or a bile duct stent, among other causes. A dilated common bile duct seen on ultrasound, in the clinical setting of fever, right upper quadrant pain, and possibly jaundice, make a very convincing case for cholangitis.

Signs and symptoms

Acute cholecystitis is comprised of right upper quadrant pain, fever, and leukocytosis associated with gallbladder inflammation. For most patients, it is caused by gallstones. There is a form of acute cholecystitis called acalculous cholecystitis where no stones are present. 

Findings on ultrasound which may suggest cholecystitis in the right clinical setting include the following[2,3]:  

  1. Thickened gall bladder wall: the anterior wall should be less than 3mm

  2. Pericholecystic fluid

  3. Presence of gall stone(s): will see shadowing behind them, make sure to check the neck of the gall bladder (may just represent biliary colic and not all cholecystitis must have stones)

  4. Sonographic Murphy’s Sign: very sensitive and with high positive predictive value [4]

If you are suspicious for bile duct involvement, specifically cholangitis, you should also consider evaluation of the common bile duct: find the portal vein, use color flow to find bile duct anterior to it. Most normal bile ducts are <4mm inside to inside with <6mm being the upper limit of normal. For patients over 50 years of age, you can add +1mm per decade to be considered in the normal range. 

Diagnosis, treatment, and prognosis

The gold standard treatment for acute cholecystitis is cholecystectomy. The timing of cholecystectomy is a matter of risk stratification. If there is sign of perforation, gangrene, or emphysema, the patient should undergo emergent cholecystectomy. If low risk and the patient is stable, the patient can undergo cholecystectomy during the hospital admission. If the patient deteriorates or does not respond to 1-3 days of antibiotics, emergent cholecystectomy is indicated. If the patient is high risk and critically ill, the attempt is made to treat with antibiotics before taking the patient to surgery.

Antibiotics are usually administered to patients presenting with acute cholecystitis, not because the process is itself infectious, per se, but as prophylaxis for possible complications including perforation, abscess, or infection of the static bile. Choice of antibiotic depends on patient risk and most likely source of possible infection.[5] 

Analgesia should progress in a stepwise fashion from NSAIDs to opioids. There is common perception that morphine causes increased Sphincter of Oddi pressure, potentially worsening pain associated with a biliary process. Morphine has not been found to cause any greater increase in pressure than any other opioid and is therefore used most commonly because of it’s less frequent dosing.[6]  

CASE RESOLUTION

The patient was admitted and treated with antibiotics, adequate pain control with morphine, and was scheduled for laparoscopic cholecystectomy. She had an uneventful post-operative course and was discharged to home from the hospital. 

TAKE-AWAYS

  • RUQ point of care ultrasound can be used to evaluate gall bladder and common bile duct pathology

  • Cholecystitis will have ultrasound findings of gall bladder wall thickening, pericholecystic fluid, and a gall stone may be visible

  • Dilation of the common bile duct can be seen with ultrasound and may point to a different biliary process such as choledocholithiasis or cholangitis with the right corresponding clinical picture

AUTHOR: Toby Nicholson is a current fourth year medical student at Alpert Medical School - Brown University.

FACULTY REVIEWER: Dr. Kristin Dwyer is the Director of Ultrasound Division of Brown Emergency Medicine

REFERENCES

  1. Kaminski DL. Arachidonic acid metabolites in hepatobiliary physiology and disease. Gastroenterology. 1989;97(3):781-792. doi:10.1016/0016-5085(89)90655-0

  2. Pinto A, Reginelli A, Cagini L, et al. Accuracy of ultrasonography in the diagnosis of acute calculous cholecystitis: review of the literature. Crit Ultrasound J. 2013;5 Suppl 1(Suppl 1):S11. doi:10.1186/2036-7902-5-S1-S11

  3. Summers SM, Scruggs W, Menchine MD, et al. A prospective evaluation of emergency department bedside ultrasonography for the detection of acute cholecystitis. Ann Emerg Med. 2010;56(2):114-122. doi:10.1016/j.annemergmed.2010.01.014

  4. Singer AJ, McCracken G, Henry MC, Thode HC Jr, Cabahug CJ. Correlation among clinical, laboratory, and hepatobiliary scanning findings in patients with suspected acute cholecystitis. Ann Emerg Med. 1996;28(3):267-272. doi:10.1016/s0196-0644(96)70024-0

  5. Gomi H, Solomkin JS, Schlossberg D, et al. Tokyo Guidelines 2018: antimicrobial therapy for acute cholangitis and cholecystitis. J Hepatobiliary Pancreat Sci. 2018;25(1):3-16. doi:10.1002/jhbp.518

  6. Thompson DR. Narcotic analgesic effects on the sphincter of Oddi: a review of the data and therapeutic implications in treating pancreatitis. Am J Gastroenterol. 2001;96(4):1266-1272. doi:10.1111/j.1572-0241.2001.03536.x